Notably, no secondary mutations in RAS, MEK, and ERK that could rebound BRAF–MEK–ERK signaling were found in PLX4720-treated TFEBS142E tumors, and no concurrent activation of the Akt–mTOR signaling pathway, previously implicated in melanoma resistance40–42, was detected in PLX4720-treated tumors (Supplementary Figs. 10d and 11e, f). Here, MTOR is linked to melanoma.